What Is Lithium Toxicity?
Lithium nephropathy is kidney damage caused by lithium preparations. Acute lithium poisoning can develop neuropsychological and muscular symptoms, including indifferent emotions, unresponsiveness, tremors, tonicity and ataxia, and possible disturbances of consciousness and coma. Acute lithium poisoning can lead to acute renal failure and a variety of kidney disorders, including chronic tubulointerstitial disease, renal diabetes insipidus and concentrating dysfunction, incomplete distal tubulic acidosis, progressive tubulointerstitial disease, and distal tubule microscopy Sac formation.
Basic Information
- English name
- lithium nephropathy
- Visiting department
- Nephrology
- Common causes
- Toxic renal damage caused by lithium preparations due to long-term lithium treatment
- Common symptoms
- Apathy, unresponsiveness, tremor, rigidity and ataxia
Causes of lithium nephropathy
- Long-term lithium treatment for toxic renal damage caused by lithium preparations.
Clinical manifestations of lithium nephropathy
- Acute lithium poisoning can develop neuropsychological and muscular symptoms, including indifferent emotions, unresponsiveness, tremors, tonicity and ataxia, and possible disturbances of consciousness and coma. Acute lithium poisoning can lead to acute renal failure and a variety of kidney disorders, including chronic tubulointerstitial disease, renal diabetes insipidus and concentrating dysfunction, incomplete distal tubulic acidosis, progressive tubulointerstitial disease, and distal tubule microscopy Sac formation. ADH-resistant urinary concentration dysfunction is reversible, and it is more common in more than 50% of patients who have been receiving lithium for a long time. Polyuria can occur in about 20% of cases. 85% of patients receiving long-term lithium treatment had normal GFR, 15% had mild GFR impairment, and a significant decrease in GFR was only seen in those who had received lithium treatment for more than 10-15 years.
Lithium nephropathy test
- Urine test
- Mild proteinuria, 24-hour urine protein quantitative <2 grams, mainly low-molecular-weight proteinuria, routine urine tests may have white blood cells, aseptic pyuria, sometimes visible microscopic hematuria or gross hematuria, urine glucose can be positive.
- 2. Renal tubule function test
- The function of urine concentration and dilution test is poor, the amino acid and bicarbonate in urine increase, uric acidification cannot reach pH 5.4, urine pH> 6, and the titratable acid in urine decreases. Urine N-acetyl--D-glucosidase (NAG) concentration increased. Patients with acute renal failure may have increased urea nitrogen and creatinine.
- 3. Other auxiliary inspections
- (1) Renal biopsy. Patients with acute renal failure related to acute lithium poisoning and patients with lithium without acute toxicity show pathological changes such as infiltration of mesenchymal leukocytes, tubule dilatation and degeneration associated with acute toxicity; and long-term lithium Interstitial fibrosis and focal tubular atrophy were seen in the treated patients. Human renal biopsy revealed characteristic pathological changes in the distal renal tubules and collecting ducts of the disease. Cell swelling and vacuole formation associated with PAS-positive glycogen accumulation were seen under light microscopy. This lesion is present in all lithium-treated patients undergoing renal biopsy, appears a few days after the start of lithium therapy, and disappears after stopping lithium therapy.
- (2) Imaging examination Urinary tract X-ray examination is not obvious in the early stage, and typical features of renal papillary necrosis appear in the later stage. X-rays of the abdomen showed changes in kidney morphology.
Diagnosis of lithium nephropathy
- The diagnosis can be confirmed based on clinical manifestations, laboratory tests, renal biopsy, and a history of long-term lithium treatment.
Differential diagnosis of lithium nephropathy
- Note that it should be distinguished from other diseases such as polyuria and thirst caused by chronic interstitial nephritis and renal diabetes insipidus.
Lithium Nephropathy Treatment
- The disease is mainly symptomatic. Polyuria and thirst caused by renal diabetes insipidus, as well as other acute manifestations of lithium damage to the kidney, often disappear quickly after the lithium preparation is discontinued. When using lithium preparations for the treatment of mental illness, consideration should be given to effectively controlling the mental illness and avoiding side effects. Polyuria can be used as an indicator of observing the side effects of lithium preparations. Care should be taken to observe the serum lithium concentration. When the lithium concentration continues to be too high or lithium toxicity repeatedly occurs, kidney damage is prone to occur. The treatment principles for patients with lithium nephropathy are the same as those for other toxic nephropathy. Discontinuation of drugs, symptomatic supportive treatment, and treatment of severe renal insufficiency should be treated as renal failure.
Prognosis of lithium nephropathy
- Most acute lithium toxic nephropathy is reversible if diagnosed promptly and the drug is stopped quickly, and the prognosis is generally good. If the diagnosis is delayed or the drug is misused again, the kidney disease can be aggravated, and the prognosis is poor when severe acute renal failure occurs. Renal biopsy has poor prognosis in patients with interstitial fibrosis and focal tubular atrophy.
Lithium Nephropathy Prevention
- It is mainly used in the treatment of mental illness with caution in the use of lithium-related preparations and other related drugs. Those who have obvious symptoms of lithium poisoning should be actively treated symptomatically to prevent more severe interstitial nephritis and kidney damage.